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. Author manuscript; available in PMC: 2020 Nov 6.
Published in final edited form as: Neuron. 2019 Sep 3;104(3):529–543.e6. doi: 10.1016/j.neuron.2019.08.001

Figure 7: Long-term potentiation in GluA1-γ−8 R8A expressing CA1 pyramidal neurons and working model of AMPAR-TARP synaptic clustering.

Figure 7:

A: Timeline of the experiment.

B: Scheme of the AMPAR replacement strategy and dual whole-cell recordings from transfected (green) and control (black) CA1 pyramidal neurons.

C: Scatterplot (left) and paired dot plot (right) of AMPAR EPSCs for single pairs (open circles) of control and Cre + GluA1-γ−8_R8A expressing cells transfected by in utero electroporation (n=13). Filled circle represents mean ± SEM. Inset shows sample current traces from control (black) and transfected (green) neurons.

D: Plots showing mean ± SEM. AMPAR EPSC amplitude of control (black) and Cre + GluA1-γ−8_R8A expressing CA1 pyramidal neurons normalized to the mean AMPAR EPSC amplitude before LTP induction (arrow). Insets shows sample current traces before (1) and 40 min after (2) LTP induction from control (black) and transfected (green) neurons. LTP induction is indicated with a gray arrow. Scale bars: 50 pA, 50 ms. Statistical significance was analyzed using the Wilcoxon signed-rank test in C. Mann–Whitney U test was used in D. * p < 0.05, ** p < 0.01.

E: A model depicting AMPAR clustering at PSD via multivalent TARP/PSD-95 interaction-mediated condensate formation by LLPS.